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Harvard researchers find that epigenetic disruptions— associated with chronic disease later in life—are already common at birth. Possibly as a result of stress on the inta-uterine environment—like maternal smoking, diet, or high levels of endocrine-disrupting chemicals.

New research suggests that a disruption of genetic imprinting often happens prenatally, implicating fetal stressors as long-term risk factor for chronic disease.

If you think stress is killing you, you may be right, but what you don't know is that stress might have harmed your health even before you were born.

In a new report appearing in the August 2013 issue of the FASEB Journal, Harvard researchers find that epigenetic disruptions, which are associated with chronic disease later in life, are already common at birth. Possibly, these aberrations result from stressors in the intrauterine environment (e.g. maternal smoking, maternal diet, or high levels of endocrine-disrupting chemicals).

This finding supports the belief that seeds of disease are sown before birth, increasing the importance of optimal prenatal care.

"This study may help us understand whether epigenetic mechanisms contribute to chronic disease susceptibility already prior to birth. We are currently exploring which stressors during prenatal life may contribute to these epigenetic disruptions," Karin Michels, Sc.D., Ph.D., study author from Harvard Medical School in Boston, Mass.

To make this discovery, Michels and colleagues examined the expression pattern of imprinted genes important for growth and development. Researchers analyzed the parental gene expression pattern in the cord blood and placenta of more than 100 infants—and followed up this analysis with methylation and expression studies. The results supported the idea that susceptibility to disease may indeed originate in utero.

Additionally, research revealed a high degree of disruption occurred during the imprinting of a gene called IGF2, expressed from both alleles in cord blood from 22 percent of study subjects.

Loss of imprinting of IGF2 has been associated with several cancers, including Wilms Tumor, colorectal and breast cancer and childhood disorders such as Beckwith-Wiedemann Syndrome.

"For a long time, doctors have considered fetal stress as a symptom of serious familial disease. Now, we see that fetal stress is in and of itself a long-term risk factor for chronic disease: it changes the way we inherit genes from our parents." Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal

AbstractImprinted genes are monoallelically expressed according to the parent of origin and are critical for proper placental and embryonic development. Disruption of methylation patterns at imprinted loci resulting in loss of imprinting (LOI) may lead to serious imprinting disorders (e.g., Beckwith-Wiedemann syndrome) and is described in some cancers (e.g., Wilms' tumor). As most research has focused on children with cancer or other abnormal phenotypes, the imprinting status in healthy infants at birth has not been characterized. We examined the prevalence of H19 and IGF2 LOI at birth by allele-specific expression assays analysis on 114 human individuals. Overall expression and methylation analyses were performed on a subset of samples. We found that LOI of H19 was observed for 4% of individuals in cord blood and 3.3% in placenta, and for IGF2 of 22% of individuals in the cord blood and 0% in placenta. Interestingly, LOI status did not correspond to aberrant methylation levels of the imprinted DMRs or with changes in overall gene expression for the majority of individuals. Our observations suggest that LOI is present in phenotypically healthy infants. Determining a “normal” human epigenotype range is important for discovering factors required to maintain a healthy pregnancy and embryonic development.—Rancourt, R. C., Harris, H. R., Barault, L., Michels, K. B. The prevalence of loss of imprinting of H19 and IGF2 at birth.

Receive monthly highlights from The FASEB Journal by e-mail. Sign up at http://www.faseb.org/fjupdate.aspx. The FASEB Journal is published by the Federation of the American Societies for Experimental Biology (FASEB). It is among the most cited biology journals worldwide according to the Institute for Scientific Information and has been recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century.

FASEB is composed of 27 societies with more than 110,000 members, making it the largest coalition of biomedical research associations in the United States. Our mission is to advance health and welfare by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.